September 1998

Alzheimer Disease–Related Abnormalities of Amyloid β Precursor Protein Isoforms in the PlateletThe Brain's Delegate in the Periphery?

Author Affiliations

Copyright 1998 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1998

Arch Neurol. 1998;55(9):1179-1180. doi:10-1001/pubs.Arch Neurol.-ISSN-0003-9942-55-9-ned7850

DURING THE last 5 years, compelling evidence has linked the deposition of β-amyloid in the neocortex to the cognitive dysfunction that characterizes Alzheimer disease (AD). The major subunit of AD-related β-amyloid is Aβ, a series of approximately 4-kd peptides found as a normal component of all biological fluids, and derived from the processing of a much larger protein, the amyloid β precursor protein (APP). Abnormalities of the processing of APP accompany all familial (autosomal dominant) forms of the disease, and transgenic models exhibiting pronounced cerebral β-amyloid deposition and some behavioral deficits have been generated by the overexpression of mutant APP. The gene for APP is on chromosome 21, and its overexpression may explain the onset of presenile Alzheimer abnormality that is an invariable complication of Down syndrome. For these reasons, there has been considerable interest in the biochemistry of APP and the possibility that abnormalities of APP processing in the brain may be reflected in the periphery, potentially serving as a diagnostic marker.

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